POS0304 THE EFFECT OF ANTI-INFLAMMATORY TREATMENT ON DEPRESSION IN SPONDYLOARTHRITIS: DOES THE TYPE OF DRUG MATTER?
Authors: C. Webers, U. Kiltz, J. Braun, D. Van der Heijde, A. Boonen
Journal: Annals of the Rheumatic Diseases (2022)

Background Patients with spondyloarthritis (SpA) are at increased risk of depression compared to the general population. Currently, it is unknown whether this increased risk is only secondary (due to SpA-related symptoms), or also due to a shared inflammatory pathway. From both clinical and pathophysiological perspectives, it is relevant to know whether comorbid depressive symptoms improve with treatment of SpA, and if so, whether such an improvement depends on drug type/mechanism of action. Objectives To investigate the effect of pharmacological treatment of SpA on depressive symptoms, and to explore whether this effect differs between drug types. Methods Data from the international ASAS Health Index Validation Study were used. Included patients had a diagnosis of SpA and fulfilled the ASAS classification criteria for axial/peripheral SpA. Patients were assessed at baseline, and for those who required a therapeutic change (initiation of NSAID, conventional synthetic (cs)DMARD or TNFi) due to high disease activity, a follow-up assessment was conducted. The current analysis included only those with a therapeutic change. Data on demographics, disease characteristics and disease activity (ASDAS, BASDAI, CRP) were available. Depressive symptoms were assessed with the depression subscale of the Hospital Anxiety and Depression Scale (HADS-D, range 0-21 [best-worst]). HADS-D scores ≥8 and ≥11 indicated possible and probable depression, respectively. Change in depressive symptoms from baseline was compared between treatments (NSAID, csDMARD, TNFi) with ANOVA and linear regression analysis, adjusting for potential confounders. Results In total, 1548 patients were assessed at baseline. A therapeutic change was initiated in 304 patients (n=102/45/157 initiated an NSAID/csDMARD/TNFi). Of these, 260 (85%) had axSpA, 190 (63%) were male, mean age was 37.3 (SD 12.6) years and mean ASDAS at baseline 3.3 (1.1). The mean HADS-D was 6.9 (4.2); 126 (42%) were possibly depressed and 66 (22%) probably depressed. At baseline, there were no significant differences in demographics, disease parameters or depressive symptoms between treatment groups. At follow-up, mean HADS-D had improved to 5.1 (change -1.9 (3.8), p&lt;0.01). Improvement in HADS-D was greater for TNFi (-2.4) than NSAIDs (-1.3, p=0.05) or csDMARDs (-1.2, p=0.15). Also, the proportion of patients with possible depression decreased more for TNFi (from 48% at baseline to 29% at follow-up) compared to NSAIDs (from 38% to 32%). In multivariable regression, initiation of TNFi was associated with greater improvement in HADS-D compared to NSAID (B = -1.27, 95%CI -2.23 to -0.32, base model) (Table 1). However, after additional adjustment for change in ASDAS/BASDAI, drug type was no longer associated with HADS-D improvement (Table 1). Adjustment for CRP in addition to BASDAI did not change results, and CRP itself was not associated with depressive symptoms (not shown). Of note, csDMARDs did not differ from NSAIDs in any of the analyses regarding their effect on HADS-D. Table 1. Multivariable regression analysis of change in HADS-D from baseline Base model ASDAS model BASDAI model Variable B 95%CI B 95%CI B 95%CI Age, years 0.04 0.00 to 0.07 0.03 -0.01 to 0.07 0.03 0.00 to 0.06 Male gender 0.23 -0.67 to 1.14 0.55 -0.39 to 1.49 0.28 -0.54 to 1.10 HLA-B27 (vs negative) Positive 1.56 0.46 to 2.67 1.38 0.27 to 2.49 1.17 0.17 to 2.18 Unknown 1.70 0.19 to 3.22 2.21 0.66 to 3.75 1.41 0.04 to 2.77 Therapy initiated (vs NSAID) csDMARD 0.19 -1.16 to 1.54 0.02 -1.34 to 1.39 0.14 -1.07 to 1.36 TNFi -1.27 -2.23 to -0.32 -0.51 -1.58 to 0.55 -0.23 -1.13 to 0.67 ASDAS, change 1.27 0.84 to 1.71 † BASDAI, change † 0.78 0.60 to 0.96 Associations in bold are statistically significant (p&lt;0.05) †Due to collinearity, ASDAS and BASDAI were tested in separate models Conclusion Treatment of active SpA also improves depressive symptoms. TNFi have a larger effect than NSAIDs, which can mainly be explained by a stronger effect on disease activity. This analysis did not find evidence for a direct link between CRP-mediated inflammation and depressive symptoms in SpA. Disclosure of Interests Casper Webers: None declared, Uta Kiltz: None declared, Juergen Braun: None declared, Désirée van der Heijde Consultant of: AbbVie, Bayer, BMS, Cyxone, Eisai, Galapagos, Gilead, Glaxo-Smith-Kline, Janssen, Lilly, Novartis, Pfizer, UCB Pharma, Employee of: Director of Imaging Rheumatology bv, Annelies Boonen Speakers bureau: Abbvie, Galapagos, Consultant of: Galapagos, Grant/research support from: Abbvie